Elevation suggests transmural injury; depression suggests subendocardial ischaemia
Mnemonic
“Elevation is a wall, depression is a layer”:
- ST elevation indicates transmural ischaemia, and localises to the territory of the occluded artery, with reciprocal depression opposite
- ST depression indicates subendocardial ischaemia, and is often widespread and non-localising
Criteria for STEMI: 1 mm in two contiguous limb leads, or 2 mm in two contiguous chest leads (1.5 mm in women), or new left bundle branch block with a compatible history.
Causes of ST elevation other than infarction: pericarditis (widespread, saddle shaped, with PR depression), early repolarisation (young, benign), left ventricular aneurysm (persistent, weeks later), Brugada, left bundle branch block and left ventricular hypertrophy (with appropriate discordance).
Widespread ST depression with elevation in aVR suggests left main or three vessel disease, and is a high risk finding.
Expansion
Ischaemic myocardium partially depolarises at rest and repolarises abnormally, generating an injury current that shifts the baseline.
- ST elevation - full thickness (transmural) injury, typically from complete occlusion of an epicardial artery
- ST depression - subendocardial ischaemia, typically from partial occlusion or from demand outstripping supply
The subendocardium suffers first for two anatomical reasons: it is at the end of the arterial tree, and it is compressed most during systole.
Other patterns worth distinguishing: reciprocal ST depression in leads opposite an infarct territory supports a true ST elevation infarct; widespread saddle-shaped elevation with PR depression suggests pericarditis; and down-sloping ST depression with a reverse tick suggests digoxin effect rather than ischaemia.